Clinicopathologic correlates in temporal cortex in dementia with Lewy bodies

Citation
T. Gomez-isla et al., Clinicopathologic correlates in temporal cortex in dementia with Lewy bodies, NEUROLOGY, 53(9), 1999, pp. 2003-2009
Citations number
43
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
NEUROLOGY
ISSN journal
00283878 → ACNP
Volume
53
Issue
9
Year of publication
1999
Pages
2003 - 2009
Database
ISI
SICI code
0028-3878(199912)53:9<2003:CCITCI>2.0.ZU;2-2
Abstract
Objective: To address the relationship between dementia and neuropathologic findings in dementia with Lewy bodies (DLB) in comparison with AD. Methods : We evaluated the clinical presentation of autopsy-confirmed DLB in compar ison with AD according to new Consortium on DLB criteria and compared the t wo conditions using quantitative neuropathologic techniques. This clinicopa thologic series included 81 individuals with AD, 20 with DLB (7 "pure" DLB and 13 "DLB/AD"), and 33 controls. We counted number of LB, neurons, senile plaques (SP), and neurofibrillary tangles (NFT) in a high order associatio n cortex, the superior temporal sulcus (STS), using stereologic counting te chniques. Results: The sensitivity and specificity of Consortium on DLB cli nical criteria in this series for dementia, hallucinations, and parkinsonis m are 53% and 83%, respectively, at the patient's initial visit and 90% and 68%, respectively, if data from all clinic visits are considered. In patho logically confirmed DLB brains, LB formation in an association cortical are a does not significantly correlate with duration of illness, neuronal loss, or concomitant AD-type pathology. Unlike AD, there is no significant neuro nal loss in the STS of DLB brains unless there is concomitant AD pathology (neuritic SP and NFT). Conclusions: The evaluation of new Consortium on DLB criteria in this series highlights their utility and applicability in clin icopathologic studies but suggests that sensitivity and specificity, especi ally at the time of the first clinical evaluation, are modest. The lack of a relationship of LB formation to the amount of Alzheimer-type changes in t his series suggests that DLB is a distinct pathology rather than a variant of AD.